I have found that treatment of cultures of rat liver epithelial cells or lung fibroblasts with the carcinogenic hydrocarbon 7, 12- dimethylbenz(a)anthracene (DMBA) has a cytotoxic effect, manifested by an inhibition of cell growth and a marked depression in acid-insoluble H3-thymidine incorporation. Within a series of methyl and ethyl- substituted benz(a)anthracenes there was an excellent correlation between reported carcinogenicity in vivo and capacity to inhibit H3- thymidine incorporation in both cultured rat liver cells and fibroblasts. Estradiol-17Beta protected rat liver epithelial cells and mouse breast epithelial cells against the DMBA inhibitory effect on H3- thymidine incorporation. Other steroids tested had little or no protective effect. A working hypothesis in that estradiol-17Beta inhibits the metabolism of DMBA to an active cytotoxic metabolite(s). Consequently, the effect of estradiol-17Beta on the rate of metabolism of H3-DMBA to water-soluble metabolites by cultured liver epithelial cells will be determined. It will also be determined if estradiol- 17Beta protects cultured epithelial cells from organs other than liver and breast against the DMBA-inhibitory effect on H3-thymidine incorporation, and if estradiol-17Beta protects against hydrocarbon carcinogens other than DMBA.